CXCL10-CXCR3 Enhances the Development of Neutrophil-mediated Fulminant Lung Injury of Viral and Nonviral Origin

Abstract

CXCL10-CXCR3 signaling appears to be a critical factor for the exacerbation of the pathology of ARDS. Thus, the CXCL10-CXCR3 axis could represent a prime therapeutic target in the treatment of the acute phase of ARDS of nonviral and viral origins.

Monoclonal antibody against CXCL-10/IP-10 ameliorates influenza A (H1N1) virus induced acute lung injury

“…A recent study demonstrated that IP-10 response enhanced the development of neutrophil-mediated fulminant lung injury of viral and non-viral origin [14]. Simi- lar to our results, they found that IP-10 was elevated in sera of patients with ARDS and the mice lacking IP-10 or CXCR3 demonstrated improved severity and survival of non-viral and viral ALI.…”

Increased Proinflammatory Responses of Monocytes and Plasmacytoid Dendritic Cells to Influenza A Virus Infection During Pregnancy

“…For example, systemic IP-10 levels were significantly elevated in serum of patients with acute respiratory distress syndrome (ARDS) induced by the seasonal 2009 influenza A(H1N1) virus, compared with patients without complications [14]. Also, in a murine model, the IP-10 and CXCR3 axis enhances the development of ARDS via the recruitment of neutrophils after pH1N1 influenza virus infection [15]. Our results and these previous discoveries suggest, that in pregnancy, influenza A virus infection leads to acute and exaggerated production of IP-10 and MIP-1β by monocytes and pDCs that could contribute to ARDS and other respiratory complications, increasing the risk of influenza-associated mortality among pregnant women.…”

CCL2 level is elevated with metabolic syndrome and CXCL10 level is correlated with visceral fat area in obese children

“…Released CCL2 caused an influx of monocytes to adipose tissue [33]. Recent studies showed that CD8 + T cells and neutrophils which have receptors for CXCL10 [34,35] infiltrated into adipose cells prior to an influx of monocytes [2,[36][37][38]. Thus, CXCL10 may attract CD8 + T cells and neutrophils before CCL2 causing the influx of monocytes.…”